Key result
Chronic intermittent hypoxia in obstructive sleep apnoea subverts the carotid body chemoreflex, causing chronic sympathetic overdrive that contributes to heart failure and resistant hypertension.
Why the study?
Chronic intermittent hypoxia in obstructive sleep apnoea disrupts carotid body chemoreflex homeostasis, leading to sympathetic overdrive and related pathophysiological consequences.
The review highlights how chronic intermittent hypoxia in obstructive sleep apnea leads to sympathetic overdrive, contributing to cardiovascular complications like heart failure and resistant hypertension.
The carotid body (CB) acts as a chemoreceptor which, when stimulated by arterial hypoxia, hypercapnia or acidosis, releases transmitters which stimulate sensory afferents that signal to the nucleus tractus solitarius (NTS). Acting through the rostral ventrolateral medulla (RVLM), this initiates a chemoreflex, stimulating autonomic efferents that orchestrate compensatory cardiorespiratory responses. Unfortunately, chronic intermittent hypoxia (CIH), which occurs in obstructive sleep apnoea (OSA), subverts the beneficial homeostatic function of this chemoreflex, causing increases in basal and hypoxia-induced transmitter release by the CB and sensitizing the cardiorespiratory centres it acts through. This causes a chronic sympathetic overdrive, contributing to the pathophysiological consequences of OSA such as heart failure, resistant hypertension and insulin resistance.
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Rocher et al. (2023) conducted a review in Obstructive sleep apnoea (OSA). Chronic intermittent hypoxia was evaluated. Chronic intermittent hypoxia in obstructive sleep apnoea subverts the carotid body chemoreflex, causing chronic sympathetic overdrive that contributes to heart failure and resistant hypertension.
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